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Autoimmune limbic encephalitis (ALE) is an inflammatory disease involving the medial temporal lobes; it classically presents with rapid neuropsychiatric decline. Patients with ALE have, and may present with, a diverse array of neuropsychiatric symptoms, which means that they may initially be assessed by any one of a range of medical practitioners. The condition was first described as a paraneoplastic phenomenon, but subsequently, with the discovery of disease-causing antibodies, was shown to be nonparaneoplastic in many cases. Although ALE is uncommon, the incidence of autoimmune encephalitides has risen over the last decade, driven largely by improved antibody detection. Autoimmune limbic encephalitis is commonly misdiagnosed, yet early diagnosis and treatment can improve outcomes. Here, Budhram et al examine the approach to diagnosis of ALE, drawing on findings of large cohort and case-control studies, which represent the highest level of evidence in this field.

In 2020, the International League Against Epilepsy (ILAE) Autoimmunity and Inflammation Taskforce introduced the terms “acute symptomatic seizures secondary to autoimmune encephalitis” and “autoimmune-associated epilepsy” to distinguish conceptually whether seizures are due to a reversible provoking factor (i.e. immunotherapy-responsive neuroinflammation) or an enduring seizure predisposition (i.e. immunotherapy-resistant neuroinflammation and/or structural injury).1 We introduced the modified term “autoimmune encephalitis-associated epilepsy” to make explicit that epilepsy is linked, either directly or indirectly, to encephalitis in all cases.2 Recently, a practical definition of AE-associated epilepsy was proposed that has important therapeutic implications, because treatment of AE-associated epilepsy focuses on anti-seizure medications (ASMs) rather than immunotherapy.3 This proposal advances the discussion of seizures related to AE. To account for uncommon patients with this subtype of AE who may initially have acute symptomatic seizures but go on to develop epilepsy, the authors proposed additional criteria that require persistent seizures following immunotherapy.3 In contrast, all patients who have seizures related to AE with antibodies against intracellular targets (e.g. most high-risk paraneoplastic antibodies, anti-glutamic acid decarboxylase-65 [GAD65]) are classified as AE-associated epilepsy, with no requirement for persistent seizures following immunotherapy.3 This is based on literature that such patients often do not attain seizure freedom following immunotherapy, indicating that the majority have immunotherapy-resistant neuroinflammation and/or structural injury causing an enduring seizure predisposition. The false equivalency results from an incomplete application of the practical definition of epilepsy.4 As per this definition, diagnosing an individual with epilepsy does not simply require that they have a seizure recurrence risk of >60%; it requires that they have a seizure recurrence risk of >60% following an unprovoked seizure, with the term “unprovoked” implying the absence of an active, reversible provoking factor.1,4 In order to apply this definition to a group, it thus follows that all individuals within that group – not simply most, but all individuals – should confidently be thought to have had at least one unprovoked seizure. The discriminatory power of an adequate immunotherapy trial Immunotherapy is an important treatment consideration for patients with AE, including those with antibodies against intracellular targets.

Abstract BACKGROUND Both stereoelectroencephalography (SEEG) and subdural strip electrodes (SSE) are used for intracranial electroencephalographic recordings in the invasive investigation of patients with drug-resistant epilepsy. OBJECTIVE To compare SEEG and SSE with respect to feasibility, complications, and outcome in this single-center study. METHODS Patient characteristics, periprocedural parameters, complications, and outcome were acquired from a pro- and retrospectively managed databank to compare SEEG and SSE cases. RESULTS A total of 500 intracranial electroencephalographic monitoring cases in 450 patients were analyzed (145 SEEG and 355 SSE). Both groups were of similar age, gender distribution, and duration of epilepsy. Implantation of each SEEG electrode took 13.9 ± 7.6 min (20 ± 12 min for each SSE; P < .01). Radiation exposure to the patient was 4.3 ± 7.7 s to a dose area product of 14.6 ± 27.9 rad*cm2 for SEEG and 9.4 ± 8.9 s with 21 ± 22.4 rad*cm2 for SSE (P < .01). There was no difference in the length of stay (12.2 ± 7.2 and 12 ± 6.3 d). The complication rate was low in both groups. No infections were seen in SEEG cases (2.3% after SSE). The rate of hemorrhage was 2.8% for SEEG and 1.4% for SSE. Surgical outcome was similar. CONCLUSION SEEG allows targeting deeply situated foci with a non-inferior safety profile to SSE and seizure outcome comparable to SSE. Graphical Abstract Graphical Abstract

To describe the experience with Anterior Nucleus of the Thalamus-Deep Brain Stimulation (ANT-DBS) for the treatment of epilepsy at a Canadian Center. All patients who underwent ANT-DBS implantation between 2013 (first patient implanted at our center) and 2020 were included. These patients had therapy-resistant epilepsy (TRE), were not candidates for resective surgery, and failed vagus nerve stimulation (VNS) treatment. Baseline of monthly seizure frequency was calculated within 3 months prior to VNS placement. Monthly seizure frequency was assessed at different points along the timeline: 3 months before ANT-DBS implantation as well as 3, 6, 12, 24, 36, 48, 60, and 72 months after ANT-DBS device placement. At each time point, seizure frequency was compared to baseline. Six patients were implanted with ANT-DBS. Three (50%) patients had multifocal epilepsy, one (16.6%) had focal epilepsy, and two (33.4%) had combined generalized and focal epilepsy. Two patients with multifocal epilepsy experienced a seizure reduction >50% in the long-term follow-up. Three (50%) patients did not showed improvement: two with combined generalized and focal epilepsy and one with focal epilepsy. There were not surgical or device-related side effects. Two (33.3%) patients presented mild and transient headaches as a stimulation-related side effect. ANT-DBS is an effective and safe treatment for focal TRE. Our experience suggests that patients with multifocal epilepsy due to regional lesion may benefit from ANT-DBS the most. Further investigations are required to determine optimal parameters of stimulation.

During that time, he also obtained a PhD in Clinical Epidemiology. In 2003, Jose and his family moved to Canada to train in Epilepsy and electroencephalography (EEG), first at the London Health Sciences Center in London, Ontario, and subsequently at the Foothills Medical Center in Calgary, Alberta. Jorge G. Burneo, Department of Clinical and Neurological Sciences and Epidemiology & Biostatistics, Western University Schulich School of Medicine and Dentistry, London, ON N6A 5C1, Canada.

A 52-year-old man in a long-term, same-gender sexual relationship presented with agitation, confusion and problems speaking for about two weeks. On assessment, his vital signs were normal, but he was agitated and had global aphasia. No other focal deficits were identified on a screening neurologic examination. He suffered a witnessed generalized tonic-clonic seizure in the emergency department and was given a loading dose of phenytoin. Seizure activity stopped, but his agitation, confusion and aphasia persisted. During that admission, he had improved without any antimicrobial or immunotherapy and been discharged with outpatient speech therapy for mild word-finding difficulties. Three months later, however, he was again admitted with agitation, confusion and aphasia. In light of the authors' experience, they suggest considering syphilis testing in patients with possible autoimmune encephalitis, especially those with temporal lobe abnormalities on neuroimaging, to avoid diagnostic delay in atypical cases such as theirs. The US Centers for Disease Control and Prevention also recommends that HIV-infected persons and sexually active men who have sex with men be screened for syphilis at least annually.

To our knowledge, EMU beds in Canada have not been previously enumerated. [...]we contacted personnel from each EMU across the country to determine the number of EMU beds available within each province and territory relative to its estimated prevalence of DRE (Table 1). Since assessment for epilepsy surgery candidacy must occur in an EMU, the insufficient number of EMU beds is a significant barrier to treating patients with DRE. Estimates of the number of epilepsy monitoring unit (EMU) beds relative to the estimated number of people with refractory epilepsy in each province and territory in Canada Province/Territory Populationa Prevalence of epilepsy per 1,000 people2 Expected number of PWEb Expected number of people with DREc Number of EMU beds Number of beds per 1,000 with DREd British Columbia 5,581,127 5.2 29,022 9,674 8 total (4 adult, 4 pediatric) 0.83 Alberta 4,756,408 5.7 27,112 9,037 10 total (8 adult, 2 pediatric) 1.11 Saskatchewan 1,218,976 5.2 6,339 2,113 None 0 Manitoba 1,465,440 4.4 6,448 2,149 3 total (2 adult, 1 pediatric) 1.40 Ontario 15,801,768 5.2 82,169 27,390 41 total (28 adult, 13 pediatric) 1.50 Quebec 8,948,540 5.4 48,322 16,107 19 total (14 adult, 5 pediatric) 1.18 New Brunswick 842,725 6.9 5,815 1,938 None 0 Nova Scotia 1,066,416 6.7 7,145 2,382 6 total (4 adult, 2 pediatric) 2.52 Prince Edward Island 175,853 4.4 774 258 None 0 Newfoundland & Labrador 540,418 6.8 3,675 1,225 None 0 Nunavut 40,817 3.7 152 51 None 0 Northwest Territories 44,760 3.7 166 56 None 0 Yukon 45,148 3.7 168 56 None 0 DRE = drug-resistant epilepsy; PWE = people with epilepsy. a Population of provinces according to Statistics Canada Q4 2023 (https://doi.org/10.25318/1710000901-eng). b Expected number of PWE calculated by multiplying population by prevalence. c Expected number of people with DRE calculated by dividing total expected number by 3. d Number of beds per 1,000 with DRE calculated by dividing the number of beds by DRE.

Background:Status epilepticus (SE) is a neurological emergency characterized by prolonged seizures. However, the incidence of first-episode SE is unclear, as estimates vary greatly among studies. Additionally, SE risk factors have been insufficiently explored. Therefore, the objectives of this study were to estimate the incidence of first-episode SE in Ontario, Canada, and estimate the associations between potential sociodemographic and health-related risk factors and first-episode SE.Methods:We conducted a population-based retrospective cohort study using linked health administrative datasets. We included individuals who completed Canada’s 2006 Census long-form questionnaire, lived in Ontario, were between 18 and 105, and had no history of SE. A Cox proportional hazards regression model was used to estimate the hazard ratios for SE within three years associated with each potential risk factor.Results:The final sample included 1,301,700 participants, 140 of whom were hospitalized or had an emergency department visit for first-episode SE during follow-up (3.5 per 100,000 person-years). Older age was the only significant sociodemographic SE risk factor (HR = 1.35, 95% CI = 1.33, 1.37), while health-related risk factors included alcohol or drug abuse (HR = 1.05, 95% CI = 1.02, 1.08), brain tumour or cancer (HR = 1.14, 95% CI = 1.12, 1.15), chronic kidney disease (HR = 1.32, 95% CI = 1.29, 1.36), dementia (HR = 1.42, 95% CI = 1.36, 1.48), diabetes (HR = 1.11, 95% CI = 1.09, 1.12), epilepsy or seizures (HR = 1.05, 95% CI = 1.01, 1.09) and stroke (HR = 1.08, 95% CI = 1.05, 1.11).Conclusion:The estimated incidence of SE in a sample of Ontario residents was 3.5 per 100,000 person-years. Older age and several comorbid conditions were associated with higher first-episode SE risk.